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December 11, 2019  
WOUNDS1 HERO

Vincent Falanga, MD: Healing Chronic Wounds


January 04, 2002

A Leader in Wound Bed Preparation


By Erin K. Blakeley, Wounds1 Staff

White paper by Dr. Falanga on wound bed preparation

Dr. Vincent Falanga is a Professor of Dermatology and Biochemistry at the Boston University School of Medicine. He also serves as Chairman of the Roger Williams Medical Center. He has authored many books on wound management and is considered a key opinion leader in the field of wound bed preparation. Wounds1 recently spoke with Dr. Falanga about wound bed management and moist wound healing.

Wounds1: What is a wound bed?

Dr. Falanga: The wound bed is what we see within the margins of a wound.

Wounds1: So the wound bed is the wound itself?

Dr. Falanga: The wound bed is bigger than the wound itself. The changes that we see in a wound are not just limited to the wound bed; instead, they are probably outside the wounded area. In other words, there are several abnormalities that exist outside the wounded area.

Wounds1: In recent years, wound management has moved to the concept of moist wound healing. Where do moist wound healing and wound bed preparation intersect?

Dr. Falanga: I am glad you bring this up. As you know, we have moved away from thinking that all wounds should be kept dry. The moist wound healing notion goes back a few thousands of years—some people knew that if you kept wounds moist, you could actually accelerate healing. Certainly, in the last couple of decades of the last century, we thought that wounds should be kept dry. Then of course, people showed that if you provided or maintained moisture, you enhanced the healing.

What is really confusing now is that as we start talking about wound bed preparation in wound management, we want to eliminate exudates (biological matter). When people hear that, they get confused. They say, on one side you are telling me that wounds need to be kept moist. On the other side, you are telling me that you need to eliminate exudates because if you have exudates, then the growth factors won’t work and the bioengineered skin will be broken down. I think that this point will need to be clarified in the future, because keeping a wound moist doesn’t necessarily mean keeping the wound exudative.

Wounds1: What is the difference?

Dr. Falanga: I think that within wounds, not all fluid is the same. Basically, I think that we need to take a concept that exists in other areas of medicine to wounds. For example, if you have fluid in other body cavities, it can be transudate, which contains very little protein and mostly water, or it can be exudate, which implies a lot of protein. We haven’t made more sophisticated differentiations clinically. We have looked at wounds and we see they are moist, they are exudative. We know when we look at a wound and it is bad, we really need to eliminate the exudate. To many people this is a source of confusion. I predict we will have to quantify and qualify what exudate is helpful in contrast to what exudate is deleterious to the process.

Wounds1: It seems that what you are describing is a delicate balance between keeping the wound moist and removing excess fluid from the wound.

Dr. Falanga: It has to do not only with the quantity that you just described, but also with the kind of exudate.

Wounds1: What is in exudate, and what differentiates different types of wound fluids?

Dr. Falanga: That is the problem—I think we haven’t defined it. We call everything an exudate and it has a negative connotation. It shouldn’t be that way. I don’t think we have enough quantification or qualification of what the wound should be. It is a source of confusion for people who are just beginning to care for wounds. When you try to tell them about moist wound healing and then you tell them that fluid is bad, it is hard for them to understand.

For the most part, the literature on moist wound healing has been developed in acute wounds, which are wounds that heal normally. That piece of information has been extrapolated to chronic wounds. The fluid that comes out of the two types of wounds are different. The fluid that comes out of an acute wound, like a surgical wound, has very different attributes than wounds that refuse to heal. There have been various characterizations of that fluid in terms of the enzymes it contains chemically and in terms of the effects that these fluids have on cells in vitro, so there is some information out there. As a group, we haven’t coalesced the information into something that makes sense for the other clinicians, or people just beginning in the field.

Wounds1: So does the reason for the difference in the quality of the exudate stem from the underlying differences between someone who is a chronic wound sufferer and someone who suffers from an acute wound?

Dr. Falanga: Yes, I think so. Not so much the general state of their health, but the local problem that caused their wound. When you have a chronic wound, is should have healed, but it hasn’t. There are some underlying reasons for that.

Wounds1: It sounds like this a particularly exciting time to be in the wound management field. What are some topics that you are in the midst of researching, as the field develops further?

Dr. Falanga: I think people have always thought about management of the wound bed as debridement. When a surgeon says is the wound bed okay, his follow up thought is that if it’s not okay, he can debride it surgically. That is really because most people deal with acute wounds. When an acute wound becomes infected, a surgeon debrides it, and what you are left with is a great wound bed—one that is ready for reepithelialization.

The problem comes with chronic wounds such as venous ulcers. You have the area that does not have skin on it, which we call the wound. Then there is the area that is hard to the touch; we call it fibrotic because it has a lot of collagen in it. There is a lot of inflammation associated with it. On top of that, because these wounds are chronic, the cells on these wounds become altered. The cellular make-up is no longer normal. The cells that try to heal or to replicate probably become old; cells can only replicate for so long. It is likely that all of these factors cause the wound not to heal.

So now, if you want to debride the wound and create a good wound bed, it will no longer be adequate. You really can’t debride inflammation. You can’t debride something that is three times the size of the ulcer in order to relieve all of the cellular abnormalities that are there.

This is where I think wound bed preparation comes into play. Most people have thought of it as debridement; but these are chronic wounds and you are not going to get at them by debridement alone. Debridement is certainly a component, but other components are there as well. Cellular abnormalities exist and these cells have to be removed. I guess you could do that by really incredible debridement. For example, you debride diabetic ulcers extensively and that helps them heal. But in many cases, you cannot.

In the future that we may talk about pharmacological agents that can modify the cells that are in wounds, kind of like chemotherapy. With cancer, you have abnormal cells that you wish to eradicate, so you administer chemotherapy. In a wound, the situation is really not that different. People have already made the connection between cancer and wounds. Obviously, wounds don’t metastasize. These chronic wounds exist on their own; they have an independence of their own. You need to tackle it in multiple ways to be able to bring about the right events that will help it heal. So I think this is where chronic wounds have gained independence form acute wounds—because they are different. It is not just about the concept that maybe you don’t need debridement every three weeks, but rather that there is ongoing necrosis in the wound. You have to think of continual debridement or “maintenance debridement” to get rid of some of the necrosis that develops all the time.

It would involve other agents, such as enzymatic agents. But we haven’t gone to this concept yet. There are some exciting areas in wound management, and many components are flawed. It is not just the fluid we need to eliminate or correct; there is also a corrupt matrix within the wound that doesn’t allow for the migration of cells across the wound bed. You have cells that are acting somewhat independently because they have gone through several replicative cycles and because of that, it is difficult for them to die. Programmed cells death becomes more difficult when a cell becomes old. Normally, cells go through this programmed cell death where they die, and that is the way it should be. But if they are very old, they are resistant to this programmed cell death, which is called apoptosis. So now you have a situation with many cells not doing the right thing, not secreting the right amount, that are not responsive to growth factors. That is why I compare them to cancer, because there is a population of cells that are going to stay there.

Wound bed preparation crystallizes many challenges we have ahead of us. It crystallizes things we have to do now to improve the situation, and also sets new goals for the future—what wound healing companies can do to create an environment conducive to indigenous wound healing.

Wounds1: What can wound sufferers do to care for their own wounds?

Dr. Falanga: One of the things that I run into a problem is the application of agents that are not prescribed. That is a big problem for us. Patients try to help themselves when they are sick. In the process of doing so they will use agents we don’t even know about, and when you ask them about it, they say no. They don’t even realize they are lying when they say no because they don’t think you are referring to lotion they may have used. They have to regard the wound bed as a very special place where the treatment you give is going to determine whether skin grows.

Last updated: 04-Jan-02

   
 
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